Proline-rich proteins (PRPs) comprise about 70% of the proteins in saliva. They can be divided into acidic, basic, and glycosylated PRPs encoded by six clustered genes on chromosome 12p13.2. PRPs are potential determinants of host susceptibility to dental caries. Large multifunctional 150-residue PRPs (Lamkin M S and Oppenheim F G, Crit Rev Oral Biol Rev 4 (1993) 251–9) are known to adsorb to hydroxyapatite surfaces and inhibit calcium phosphate precipitation, modulate hydroxyapatite crystal formation as well as mediate adhesion of commensal Actinomyces and Streptococcus species to tooth surfaces. In addition, they bind to and inactivate ingested plant polyphenols (tannins). The proline-poor N-terminal 30 residue domain confers hydroxyapatite- and calcium-binding, while the proline-rich middle/C-terminal domain binds bacteria via the ProGln-terminus and tannins via proline-rich repeats.
The polymorphism of acidic PRPs involves allelic and post-translational variants; several common allelic (large PRP-1, PRP-2, Db-s, PIF-s and Pa) and post-translational (small PRP-3, PRP-4, Db-f and PIF-f) variants have been described. In regard of biological properties the acidic PRP variants differ somewhat, and large and small acidic PRPs largely, between each other. The small 106 residue acidic PRPs resulting from proteolytic cleavage at Arg106-Gly107 display poor bacterial adhesion activity but high affinity for hydroxyapatite surfaces. Both large and small acidic PRPs are secreted from the acinus cells. After secretion, the acidic PRPs are rapidly enriched on tooth surfaces and degraded as a consequence of bacterial proteolysis. Also, multiple phosphorylated peptides reminiscent of PRPs have been identified in saliva and found to possess increased affinity for hydroxyapatite surfaces. Some studies (Kousvelari E E et al., J Dent Res 59 (1980) 1430–8), though not others (Mandel I D & Bennick A, J Dent Res 62 (1980) 943–5), have associated this proteolytic activity to gingivitis and rate of plaque formation.
Arg catabolism to ammonia has been suggested to be a characteristic of streptococcal biotypes with tooth protective properties (Andersson C et al. Infect Immun 43 (1984) 555–60; Rogers A H, Aust Dent J 35 (1990) 468–71. Wijeyeweera R L& Kleinberg, Arch Oral Biol 34 (1989) 55–64; ibid. 43–53). Actually, Arg can control the ecological relationship between S. sanguis and S. mutans (van der Hoeven J S et al., J Dent Res 63 (1984) 389–92. Rogers A H et al., Oral Microbiol Immunol 2 (1987) 172–82), and caries-susceptible and caries-resistant subjects differ in ability to raise pH after an acidification (Abelson D C & Mandel I D, J Dent Res 60 (1981) 1634–8; Kleinberg I et al., Proc. “Microbial aspects of dental caries”. Sp. Supp. Microbiol. Abstracts. IRL, Washington, D.C., 1976, 433–464 pp).
Arg catabolism is present in S. sanguis, S. gordonii, S. anginosus and S. mitis, while it is absent in S. oralis and cariogenic S. mutans and S. sobrinus (Kilian M et al., Int J Syst Bacteriol 39 (1989) 471–484). Arg-containing peptides, notably sialin (Coulter W A et al., Biochem Soc Trans 18 (1990) 337–8) may act as a local pH-buffering agents by bacterial catabolism of Arg to ammonia via the arginine deaminase pathway (Floderus E et al., APMIS 98 (1990) 1045–52).
Degradation of acidic PRPs releases oligopeptides which are transported intra-cellularly and metabolized for nutritional reasons (Kunji E R et al., Antonie Van Leeuwenhoek 70 (1996) 187–221). Gram-negative bacteria colonizing the gingival pocket, such as Porphyromonas gingivalis, express a broad range of proteases in utilizing proteins as a major source of energy. In contrast, commensal streptococci and actinomycetes, which dominate on oral mucosal and tooth surfaces, express multiple glycosidases in utilizing carbohydrates as a major energy source. Nevertheless, protease and peptidase activities, such as a trypsin-like serine endoprotease in S. oralis, S-IgA1 proteases in S. sanguis and S. oralis and yet uncharacterized proteolytic activity, are present in Streptococcus and Actinomyces species. However, little is known about the degradation of acidic PRPs by these commensal and early colonizing bacteria.
While a vast amount of knowledge about saliva constitutents and their possible role in processes leading to dental caries has been gathered, that knowledge up to know resulted in only few practically applicable propositions of how to efficiently prevent dental caries.